Maintained barostatic regulation of heart rate in digesting snakes (Boa constrictor)

When snakes digest large meals, heart rate is accelerated by withdrawal of vagal tone and an increased non-adrenergic-non-cholinergic tone that seems to stem from circulating blood-borne factors exerting positive chronotropic effects. To investigate whether this tonic elevation of heart rate impairs the ability for autonomic regulation of heart during digestion, we characterised heart rate responses to pharmacological manipulation of blood pressure in the snake Boa constrictor through serial injections of sodium nitroprusside and phenylephrine. Both fasting and digesting snakes responded with a robust tachycardia to hypotension induced by sodium nitroprusside, with digesting snakes attaining higher maximal heart rates than fasting snakes. Both fasting and digesting snakes exhibited small reductions of the cardiac chronotropic response to hypertension, induced by injection of phenylephrine. All heart rate changes were abolished by autonomic blockade with the combination of atropine and propranolol. The digesting snakes retained the capacity for compensatory heart rate responses to hypotension, despite their higher resting values, and the upward shift of the barostatic response curve enable snakes to maintain the cardiac limb for blood pressure regulation.

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Autonomic control of heart rate during forced activity and digestion in the snakeBoa constrictor

Journal of Experimental Biology ◽

10.1242/jeb.204.20.3553 ◽

2001 ◽

Vol 204 (20) ◽

pp. 3553-3560 ◽

Cited By ~ 2

Author(s):

Tobias Wang ◽

E. W. Taylor ◽

Denis Andrade ◽

Augusto S. Abe

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiovascular Responses ◽

Autonomic Control ◽

Boa Constrictor ◽

Adrenergic Antagonist ◽

Autonomic Blockade ◽

The Mean ◽

Positive Chronotropic Effect ◽

Mean Heart Rate

SUMMARYReptiles, particularly snakes, exhibit large and quantitatively similar increments in metabolic rate during muscular exercise and following a meal, when they are apparently inactive. The cardiovascular responses are similar during these two states, but the underlying autonomic control of the heart remains unknown. We describe both adrenergic and cholinergic tonus on the heart during rest, during enforced activity and during digestion (24–36 h after ingestion of 30 % of their body mass) in the snake Boa constrictor. The snakes were equipped with an arterial catheter for measurements of blood pressure and heart rate, and autonomic tonus was determined following infusion of the β-adrenergic antagonist propranolol (3 mg kg–1) and the muscarinic cholinoceptor antagonist atropine (3 mg kg–1).The mean heart rate of fasting animals at rest was 26.4±1.4 min–1, and this increased to 36.1±1.4 min–1 (means ± s.e.m.; N=8) following double autonomic block (atropine and propranolol). The calculated cholinergic and adrenergic tones were 60.1±9.3 % and 19.8±2.2 %, respectively. Heart rate increased to 61.4±1.5 min–1 during enforced activity, and this response was significantly reduced by propranolol (maximum values of 35.8±1.6 min–1), but unaffected by atropine. The cholinergic and adrenergic tones were 2.6±2.2 and 41.3±1.9 % during activity, respectively. Double autonomic block virtually abolished tachycardia associated with enforced activity (heart rate increased significantly from 36.1±1.4 to 37.6±1.3 min–1), indicating that non-adrenergic, non-cholinergic effectors are not involved in regulating heart rate during activity. Blood pressure also increased during activity.Digestion was accompanied by an increase in heart rate from 25.6±1.3 to 47.7±2.2 min–1 (N=8). In these animals, heart rate decreased to 44.2±2.7 min–1 following propranolol infusion and increased to 53.9±1.8 min–1 after infusion of atropine, resulting in small cholinergic and adrenergic tones (6.0±3.5 and 11.1±1.1 %, respectively). The heart rate of digesting snakes was 47.0±1.0 min–1 after double autonomic blockade, which is significantly higher than the value of 36.1±1.4 min–1 in double-blocked fasting animals at rest. Therefore, it appears that some other factor exerts a positive chronotropic effect during digestion, and we propose that this factor may be a circulating regulatory peptide, possibly liberated from the gastrointestinal system in response to the presence of food.

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Blood pressure regulation by ETA and ETB receptors in conscious, telemetry-instrumented mice and role of ETA in hypertension produced by selective ETB blockade

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01221.2005 ◽

2006 ◽

Vol 290 (6) ◽

pp. H2554-H2559 ◽

Cited By ~ 14

Author(s):

Ryan M. Fryer ◽

Pamela A. Rakestraw ◽

Patricia N. Banfor ◽

Bryan F. Cox ◽

Terry J. Opgenorth ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Blood Pressure Regulation ◽

Pressure Regulation ◽

Type B ◽

Selective Antagonist ◽

Relevant Role ◽

Basal Blood Pressure ◽

Baseline Values

The net contribution of endothelin type A (ETA) and type B (ETB) receptors in blood pressure regulation in humans and experimental animals, including the conscious mouse, remains undefined. Thus we assessed the role of ETA and ETB receptors in the control of basal blood pressure and also the role of ETA receptors in maintaining the hypertensive effects of systemic ETB blockade in telemetry-instrumented mice. Mean arterial pressure (MAP) and heart rate were recorded continuously from the carotid artery and daily (24 h) values determined. At baseline, MAP ranged from 99 ± 1 to 101 ± 1 mmHg and heart rate ranged between 547 ± 15 and 567 ± 19 beats/min ( n = 6). Daily oral administration of the ETB selective antagonist A-192621 [10 mg/kg twice daily] increased MAP to 108 ± 1 and 112 ± 2 mmHg on days 1 and 5, respectively. Subsequent coadministration of the ETA selective antagonist atrasentan (5 mg/kg twice daily) in conjunction with A-192621 (10 mg/kg twice daily) decreased MAP to baseline values on day 6 (99 ± 2 mmHg) and to below baseline on day 8 (89 ± 3 mmHg). In a separate group of mice ( n = 6) in which the treatment was reversed, systemic blockade of ETB receptors produced no hypertension in animals pretreated with atrasentan, underscoring the importance of ETA receptors to maintain the hypertension produced by ETB blockade. In a third group of mice ( n = 10), ETA blockade alone (atrasentan; 5 mg/kg twice daily) produced an immediate and sustained decrease in MAP to values below baseline (baseline values = 101 ± 2 to 103 ± 2 mmHg; atrasentan decreased pressure to 95 ± 2 mmHg). Thus these data suggest that ETA and ETB receptors play a physiologically relevant role in the regulation of basal blood pressure in normal, conscious mice. Furthermore, systemic ETB receptor blockade produces sustained hypertension in conscious telemetry-instrumented mice that is absent in mice pretreated with an ETA antagonist, suggesting that ETA receptors maintain the hypertension produced by ETB blockade.

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Regulation of arterial blood pressure in Australian tiger snakes

Journal of Experimental Biology ◽

10.1242/jeb.75.1.65 ◽

1978 ◽

Vol 75 (1) ◽

pp. 65-79 ◽

Cited By ~ 7

Author(s):

H. B. Lillywhite ◽

R. S. Seymour

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Complete Recovery ◽

Pressure Control ◽

Pressure Regulation ◽

Body Temperatures ◽

Heating And Cooling ◽

Arterial Blood ◽

Preferred Temperatures ◽

Head Up Tilt

1. Blood pressure was measured in the dorsal aorta of restrained, unanaesthetized tiger snakes (Notechis scutatus) at different body temperatures during graded, passive tilt. Aortic blood pressure in horizontal snakes showed no significant change over a range of body temperatures between 18 and 33 degrees C (mean of measurements on 16 snakes = 42.2 +/− I.98 mmHg), while heart rate increased logarithmically (Q10 approximately 2.5). Blood pressure was stable during heating and cooling between body temperatures of 15 and 30 degrees C, but the pressure was 10--50% higher during heating than during cooling. 2. Head-up tilt usually caused a brief fall in pressure at heart level followed by partial or complete recovery and tachycardia. At the cessation of tilt, there was a characteristic overshoot of the blood pressure followed by readjustment to control (pretilt) levels. Head-down tilt typically increased pressure which then either stabilized or returned toward pretilt levels. Heart rate changes during head-down tilt were not consistent in direction or magnitude. Stabilized pressures at mid-body usually increased following head-up tilt and decreased following head-down tilt, indicating physiological adjustment to posture change. Blood pressure control was evident at body temperatures ranging from 10 to 38 degrees C, but was most effective at the higher and behaviourally preferred temperatures. 3. Propranolol lowered heart rate but did not influence pressure in horizontal snakes. During head-up tilt propranolol eliminated or reduced tachycardia and sometimes reduced the efficacy of pressure compensation for tilt. Phentolamine increased heart rate, lowered blood pressure, and eliminated pressure regulation during tilt. The results suggest that sympathetically mediated reflexes assist central blood pressure regulation in the tiger snake, with vasomotor adjustments having greater importance than changes in heart rate.

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The Central Effect of Physostigmine on Blood Pressure and Heart Rate; Possible Cholinerg Aspects of Blood Pressure Regulation

Deutsche Pharmakologische Gesellschaft ◽

10.1007/978-3-662-39532-5_156 ◽

1978 ◽

pp. 39-39

Author(s):

D. de Wildt ◽

A. J. Porsius

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Blood Pressure Regulation ◽

Central Effect ◽

Pressure Regulation

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Baroreflex modulation of heart rate and initiation of atrial activation in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.3.h503 ◽

1988 ◽

Vol 255 (3) ◽

pp. H503-H513 ◽

Cited By ~ 1

Author(s):

R. B. Schuessler ◽

T. E. Canavan ◽

J. P. Boineau ◽

J. L. Cox

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Right Atrial ◽

Autonomic Blockade ◽

Left And Right ◽

Atrial Activation ◽

The Right ◽

A Site ◽

Induced Changes ◽

Cardiac Nerves

In open-chest dogs, blood pressure was regulated by titrating doses of phenylephrine and nitroprusside to determine its effect on heart rate and pacemaker location. Changes in blood pressure correlated with changes in heart rate (r = 0.86). Activation time mapping demonstrated multicentric atrial activation, with a site of origin-rate relationship. The fastest pacemakers were located in the most cranial regions and slowest in the most caudal areas. In this chloralose-morphine anesthetized model, autonomic blockade with atropine and propranolol suggests that acute baroreflex-induced changes in heart rate were mediated exclusively by either increased sympathetic or parasympathetic tone and were not associated with inhibition of the opposite system. Division of right and left thoracic cardiac nerves indicated the left sympathetics participated in the baroreflex in 50% of the animals and the left parasympathetics in 90% of the animals. Both the right sympathetics and parasympathetics were active in the baroreflex in all animals. The data demonstrate that physiological heart rate response is regulated through an extensive system of right atrial pacemakers modulated by both left and right efferent cardiac nerves.

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Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1983.244.1.r74 ◽

1983 ◽

Vol 244 (1) ◽

pp. R74-R77 ◽

Cited By ~ 3

Author(s):

J. Schwartz ◽

I. A. Reid

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Plasma Renin Activity ◽

Water Deprivation ◽

Plasma Renin ◽

Renin Activity ◽

Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

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ON THE HYPERTENSIVE ACTION OF TOLAZOLINE AND HYDERGINE

Canadian Journal of Biochemistry and Physiology ◽

10.1139/y63-106 ◽

1963 ◽

Vol 41 (1) ◽

pp. 941-946 ◽

Cited By ~ 1

Author(s):

B. G. Benfey ◽

D. R. Varma

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Contractility ◽

Pressure Rise ◽

Pressor Effect ◽

Blood Pressure Rise ◽

Chronotropic Effects

The effects of tolazoline and Hydergine on blood pressure, cardiac contractility, and heart rate have been studied in dogs under pentobarbitone anesthesia. Whereas in the absence of reserpine, tolazoline had a pressor effect in two of four dogs, following reserpine it had a marked pressor action in each of eight dogs. The blood pressure rise was associated with positive inotropic and negative chronotropic effects. Phenoxybenzamine abolished these effects of tolazoline. Hydergine had pressor and negative chronotropic effects in the absence of reserpine. Following reserpine these effects were associated with positive inotropic actions. Phenoxybenzamine reduced these effects of Hydergine. It is concluded that the pressor action of tolazoline is wholly due to adrenergic vasoconstriction, whereas that of Hydergine is only partly an adrenergic effect.

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Afferent vascular resistance control during hemorrhage in normal and autonomically blocked rabbits

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.2.h380 ◽

1991 ◽

Vol 261 (2) ◽

pp. H380-H391 ◽

Cited By ~ 5

Author(s):

C. A. Courneya ◽

P. I. Korner ◽

J. R. Oliver ◽

R. L. Woods

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Afferent Input ◽

Ang Ii ◽

Local Response ◽

Simple Addition ◽

Autonomic Blockade ◽

The Difference ◽

Constrictor Response

We examined the role of the arterial and cardiac baroreceptors on the hindquarter conductance and heart rate responses of conscious rabbits bled at approximately 3% blood volume (BV)/min to 80% BV (i.e., 20% BV removed). We used rabbits with both sets of baroreceptors working and when only one or neither sets was working. Each animal was studied with normal effector function and during autonomic blockade (hormonal + local effectors), where release of arginine vasopressin (AVP) and renin (angiotensin II, ANG II) were enhanced. The local response (LR) to hemorrhage was determined in a separate group of neurohumorally blocked rabbits. The estimated constrictor response (ECR) was the difference between the LR and net conductance response. In normal rabbits, the ECR was 49 units, with the estimated arterial-to-cardiac barorecptor drive ratio approximately 2.8:1 and with the two receptor groups acting by simple addition. Both barorecptors contributed to the rise in heart rate, with the relative arterial-to-cardiac baroreceptor drive ratio approximately 4:1. When hemorrhage was performed during autonomic blockade, ECR was 84 units (compared with normal rabbits, P less than 0.01), but blood pressure was poorly maintained and the constrictor effect was not under baroreceptor control. Although the baroreceptors were critical for AVP release during autonomic blockade, they played no role in renin release (ANG II production); the latter was released in large amounts, producing near-maximum constriction, which was unrelated to the afferent input. Thus neurally mediated regulation during hemorrhage has substantial advantages over that mediated primarily through the pressor hormones.

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Effect of ‘Autonomic Blockade’ on Cardiac β-Adrenergic Chronotropic Responsiveness in Healthy Young, Healthy Elderly and Endurance-Trained Elderly Subjects

Clinical Science ◽

10.1042/cs0870297 ◽

1994 ◽

Vol 87 (3) ◽

pp. 297-302 ◽

Cited By ~ 15

Author(s):

G. A. Ford ◽

O. F. W. James

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Geometric Mean ◽

Cardiovascular Responses ◽

The Elderly ◽

Elderly Subjects ◽

Healthy Elderly ◽

Age Related ◽

Autonomic Blockade ◽

Young Subjects

1. Cardiac chronotropic responses to isoprenaline are reduced with ageing in man. It is unclear whether this is due to reduced cardiac β-adrenergic sensitivity or to age-associated differences in reflex cardiovascular responses to the vasodilatory effects of isoprenaline. Age-associated changes in physical activity are also reported to influence β-adrenergic sensitivity. 2. The aim of the present study was to determine the contribution of alterations in reflex changes in parasympathetic and sympathetic influences and physical fitness to the age-associated reduction in cardiac chronotropic responses to β-adrenergic agonists. 3. The effect of ‘autonomic blockade’ with atropine (40 μg/kg intravenously) and clonidine (4 μg/kg intravenously) on blood pressure, heart rate and chronotropic responses to intravenous bolus isoprenaline doses was determined in eight healthy young (mean age 21 years), nine healthy elderly (72 years) and 10 endurance-trained elderly (69 years) subjects. 4. Elderly subjects had a reduced increase in heart rate after atropine (young, 49 ± 9 beats/min; elderly, 36 ± 5 beats/min; endurance-trained elderly, 34 ± 12 beats/min; P < 0.01) and did not demonstrate the transient increase in systolic blood pressure after clonidine observed in young subjects (young, 11 ± 10 mmHg; elderly, −12 ± 16 mmHg; endurance-trained elderly, −18 ± 11 mmHg; P < 0.01). 5. Cardiac chronotropic sensitivity to isoprenaline after ‘autonomic blockade’ increased in the young but decreased in the elderly subjects. The isoprenaline dose that increased heart rate by 25 beats/min before and after autonomic blockade' was: young, before 1.6 μg, after 2.8 μg, P < 0.01 (geometric mean, paired test); elderly, before 6.9 μg, after 3.6 μg, P < 0.05; endurance-trained elderly, before 5.9 μg, after 4.0 μg, P < 0.05. Cardiac chronotropic sensitivity to isoprenaline was significantly reduced in elderly compared with young subjects before (P < 0.01) but was similar after (P = 0.09) ‘autonomic blockade’. Chronotropic sensitivity did not differ between healthy and endurance-trained elderly subjects before or after ‘autonomic blockade’. 6. The age-associated reduction in cardiac chronotropic responses to bolus isoprenaline is primarily due to an age-related reduction in the influence of reflex cardiovascular responses on heart rate and not to an age-related reduction in cardiac β-adrenergic sensitivity. Endurance training is not associated with altered β-adrenergic chronotropic sensitivity in the elderly. The transient pressor response to intravenously administered clonidine may be lost in ageing man.

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